Right ventricular dysfunction and the exercise limitation of chronic obstructive pulmonary disease

This study examined right ventricular function during exercise in patients with chronic obstructive pulmonary disease to answer the following questions: Is there a significant correlation between oxygen consumption at maximal exercise and exercise right ventricular ejection fraction? Does the right ventricular ejection fraction response to exercise correlate with exercise changes in pulmonary artery pressure, total pulmonary resistance or pulmonary vascular resistance? Which combinations of cardiac, ventilatory and blood gas variables are the best predictors of oxygen consumption at maximal exercise? Twenty-six patients with stable chronic obstructive pulmonary disease performed symptom-limited supine bicycle exercise with simultaneous hemodynamic and radionuclide ventriculographic measurements. The oxygen consumption at maximal exercise correlated with the exercise right ventricular ejection fraction (n = 21, r = 0.66; p less than 0.005), exercise stroke volume (r = 0.68; p less than 0.001), exercise cardiac output (r = 0.77; p less than 0.00005) and exercise ventilation (r = 0.85; p less than 0.00001). The change in right ventricular ejection fraction from rest to exercise correlated inversely with the change from rest to exercise in total pulmonary resistance (r = -0.51; p less than 0.05) but not with the change in mean pulmonary pressure (r = -0.37) or in pulmonary vascular resistance (r = 0.09). Multivariate analysis showed that the variables giving the highest combined correlation with oxygen consumption were ventilation and right ventricular ejection fraction (r = 0.95, adjusted r2 = 0.88). These results suggest that exercise oxygen consumption of patients with chronic obstructive pulmonary disease is related to right ventricular systolic function, exercise right ventricular dysfunction is related, in part, to abnormal exercise total pulmonary resistance, and exercise limitation in chronic obstructive pulmonary disease occurs as a result of the dynamic interaction between disordered right heart function and ventilation.

This article has been cited by other articles:

				H. Rietema, S. Holverda, H. J. Bogaard, J. T. Marcus, H. J. Smit, N. Westerhof, P. E. Postmus, A. Boonstra, and A. Vonk-Noordegraaf Sildenafil treatment in COPD does not affect stroke volume or exercise capacity Eur. Respir. J., April 1, 2008; 31(4): 759 - 764. [Abstract] [Full Text] [PDF]

				F. Gigliotti, C. Coli, R. Bianchi, I. Romagnoli, B. Lanini, B. Binazzi, and G. Scano Exercise Training Improves Exertional Dyspnea in Patients With COPD: Evidence of the Role of Mechanical Factors Chest, June 1, 2003; 123(6): 1794 - 1802. [Abstract] [Full Text] [PDF]

				F. Maltais, J. Jobin, M. J. Sullivan, S. Bernard, F. Whittom, K. J. Killian, M. Desmeules, M. Belanger, and P. LeBlanc Metabolic and hemodynamic responses of lower limb during exercise in patients with COPD J Appl Physiol, May 1, 1998; 84(5): 1573 - 1580. [Abstract] [Full Text] [PDF]